中华传染病杂志
中華傳染病雜誌
중화전염병잡지
CHINESE JOURNAL OF INFECTIOUS DISEASES
2001年
2期
73-76
,共4页
王静艳%穆桂玲%刘沛%谷秋红
王靜豔%穆桂玲%劉沛%穀鞦紅
왕정염%목계령%류패%곡추홍
肝炎,乙型%T淋巴细胞亚群%细胞因子%变异
肝炎,乙型%T淋巴細胞亞群%細胞因子%變異
간염,을형%T림파세포아군%세포인자%변이
目的 探讨在重型肝炎中,乙型肝炎病毒(HBV)前C区1896位基因突变与机体免疫水平的关系。方法 采用限制性酶切片段长度多态性分析(RFLP)检测HBV基因组前C区1896位是否存在变异,以单克隆抗体APAAP法比较末梢血T细胞亚群的分布情况,用双抗体夹心ELISA法检测血清细胞因子(TNF-a、IFN-γ、IL-6、IL-8)水平。结果 23例重型肝炎中,HBV基因变异株感染率为52 2%,而22例急性乙型肝炎中仅1例为变异株感染;变异株组CD8+T细胞百分率明显下降,CD4+/CD8+比值明显增高,CD3+、CD4+T细胞的百分率未见明显变化;重型肝炎中细胞因子(TNF-a、IFN-γ、IL-6、IL-8)水平均明显高于急性乙型肝炎相应之细胞因子水平,而变异株组IFN-γ、IL-6水平明显高于非变异株组,TNF-a和IL-8在两组间无明显差异;变异株组病死率(100%)明显高于野毒株组的病死率(9%)。结论 重型肝炎中,变异株HBV感染率很高;基因变异的HBV可能通过各种途径刺激机体的免疫系统,使免疫细胞活化,从而释放大量细胞因子,导致肝细胞损伤,甚至肝衰竭。
目的 探討在重型肝炎中,乙型肝炎病毒(HBV)前C區1896位基因突變與機體免疫水平的關繫。方法 採用限製性酶切片段長度多態性分析(RFLP)檢測HBV基因組前C區1896位是否存在變異,以單剋隆抗體APAAP法比較末梢血T細胞亞群的分佈情況,用雙抗體夾心ELISA法檢測血清細胞因子(TNF-a、IFN-γ、IL-6、IL-8)水平。結果 23例重型肝炎中,HBV基因變異株感染率為52 2%,而22例急性乙型肝炎中僅1例為變異株感染;變異株組CD8+T細胞百分率明顯下降,CD4+/CD8+比值明顯增高,CD3+、CD4+T細胞的百分率未見明顯變化;重型肝炎中細胞因子(TNF-a、IFN-γ、IL-6、IL-8)水平均明顯高于急性乙型肝炎相應之細胞因子水平,而變異株組IFN-γ、IL-6水平明顯高于非變異株組,TNF-a和IL-8在兩組間無明顯差異;變異株組病死率(100%)明顯高于野毒株組的病死率(9%)。結論 重型肝炎中,變異株HBV感染率很高;基因變異的HBV可能通過各種途徑刺激機體的免疫繫統,使免疫細胞活化,從而釋放大量細胞因子,導緻肝細胞損傷,甚至肝衰竭。
목적 탐토재중형간염중,을형간염병독(HBV)전C구1896위기인돌변여궤체면역수평적관계。방법 채용한제성매절편단장도다태성분석(RFLP)검측HBV기인조전C구1896위시부존재변이,이단극륭항체APAAP법비교말소혈T세포아군적분포정황,용쌍항체협심ELISA법검측혈청세포인자(TNF-a、IFN-γ、IL-6、IL-8)수평。결과 23례중형간염중,HBV기인변이주감염솔위52 2%,이22례급성을형간염중부1례위변이주감염;변이주조CD8+T세포백분솔명현하강,CD4+/CD8+비치명현증고,CD3+、CD4+T세포적백분솔미견명현변화;중형간염중세포인자(TNF-a、IFN-γ、IL-6、IL-8)수평균명현고우급성을형간염상응지세포인자수평,이변이주조IFN-γ、IL-6수평명현고우비변이주조,TNF-a화IL-8재량조간무명현차이;변이주조병사솔(100%)명현고우야독주조적병사솔(9%)。결론 중형간염중,변이주HBV감염솔흔고;기인변이적HBV가능통과각충도경자격궤체적면역계통,사면역세포활화,종이석방대량세포인자,도치간세포손상,심지간쇠갈。
Objective To study the relationship between the HBV precore 1896 site mutation and the host immunity. Methods HBV precore 1896 site mutation was confirmed by restriction fragment length polymorphism analysis; The cytokines (TNF-a、 IFN-γ、 IL-6 and IL-8) levels were measured by enzyme linked immunosorbent assay(ELISA) and T subpopulations by APAAP. Results In fulminant hepatitis, the infective rate of HBV mutate-type was 52.5 %, while only one patient was infected by mutate-type virus in acute hepatitis; The percentage of CD8 +T lymphocyte was obviously lower and the ratio of CD4+/CD8+ was obviously higher in mutate group than wild strain group; The cytokine levels in the patients with fulminant hepatitis were higher than those in acute hepatitis. The mortality of patients with mutate-type was higher ( 100 % ) than that of wild-type (9 % ). Conclusion In fulminant hepatitis, the infective rate of HBV mutate-type is high. The mutate-type virus provokes host immune system resulting in the activation of lymphocyte and release of cytokines, which contributed to severe liver damage.